Positions

Overview

  • Ashley Cannon, PhD, MS, CGC is an Assistant Professor at UAB in the Department of Genetics. She is a neuroscientist and certified genetic counselor. Her previous research experience at Mayo Clinic Florida encompassed molecular genetics, neuropathology, and mouse modeling of neurodegenerative diseases. This research exposed her to the significance of genetic counseling for individuals and families affected by genetic conditions and motivated her to become trained as a genetic counselor. She received an MS in Genetic Counseling at UAB in 2015. She currently provides genetic counseling for the Neurofibromatosis Clinic and Undiagnosed Diseases Program. Her current research interests include the longitudinal quantification, treatment, and psychosocial impact of cutaneous neurofibromas in individuals with NF1.

    • Selected Publications

    Academic Article

    Year Title Altmetric
    2021 Perspective of Adults With Neurofibromatosis 1 and Cutaneous Neurofibromas: Implications for Clinical Trials.  Neurology.  97:S15-S24. 2021
    2020 Genetic Counseling for Neurofibromatosis 1, Neurofibromatosis 2, and Schwannomatosis—Practice Resource of the National Society of Genetic Counselors.  Journal of Genetic Counseling.  29:692-714. 2020
    2019 Expanding the clinical phenotype of individuals with a 3-bp in-frame deletion of the NF1 gene (c.2970_2972del): an update of genotype–phenotype correlation.  Genetics in Medicine.  21:867-876. 2019
    2019 Correction to: Expanding the clinical phenotype of individuals with a 3-bp in-frame deletion of the NF1 gene (c.2970_2972del): an update of genotype–phenotype correlation (Genetics in Medicine, (2018), 10.1038/s41436-018-0269-0).  Genetics in Medicine.  21:764-765. 2019
    2018 Clinical trial design for cutaneous neurofibromas.  Neurology.  91:S31-S37. 2018
    2018 Unusual presentation of hereditary leiomyomatosis mimicking neurofibromatosis.  JAAD Case Reports.  4:440-441. 2018
    2018 Cutaneous neurofibromas in Neurofibromatosis type I: A quantitative natural history study.  Orphanet Journal of Rare Diseases.  13. 2018
    2016 Advanced Genetic Testing Comes to the Pain Clinic to Make a Diagnosis of Paroxysmal Extreme Pain Disorder..  Case Reports in Neurological Medicine.  2016:9212369. 2016
    2015 Clinicopathologic and 11C-Pittsburgh compound B implications of Thal amyloid phase across the Alzheimer's disease spectrum 2015
    2014 Concurrent variably protease-sensitive prionopathy and amyotrophic lateral sclerosis.  Acta Neuropathologica.  128:313-315. 2014
    2014 Divergent phenotypes in mutant TDP-43 transgenic mice highlight potential confounds in TDP-43 transgenic modeling.  PLoS One.  9. 2014
    2014 Differential clinicopathologic and genetic features of late-onset amnestic dementias.  Acta Neuropathologica.  128:411-421. 2014
    2013 Unbiased screen reveals ubiquilin-1 and -2 highly associated with huntingtin inclusions.  Brain Research.  1524:62-73. 2013
    2013 Robust cytoplasmic accumulation of phosphorylated TDP-43 in transgenic models of tauopathy.  Acta Neuropathologica.  126:39-50. 2013
    2013 Clinicopathologic variability of the GRN A9D mutation, including amyotrophic lateral sclerosis.  Neurology.  80:1771-1777. 2013
    2012 Neuronal sensitivity to TDP-43 overexpression is dependent on timing of induction.  Acta Neuropathologica.  123:807-823. 2012
    2008 Risk-reducing effect of education in Alzheimer's disease.  International Journal of Geriatric Psychiatry.  23:1156-1162. 2008
    2008 APOE ε4 lowers age at onset and is a high risk factor for Alzheimer's disease; A case control study from central Norway.  BMC Neurology.  8. 2008
    2008 Cholesterol-related genetic risk scores are associated with hypometabolism in Alzheimer's-affected brain regions.  NeuroImage.  40:1214-1221. 2008
    2008 Study of a Swiss dopa-responsive dystonia family with a deletion in GCH1: Redefining DYT14 as DYT5.  Neurology.  70:1377-1383. 2008
    2007 Progranulin mutations and amyotrophic lateral sclerosis or amyotrophic lateral sclerosis-frontotemporal dementia phenotypes.  Journal of Neurology, Neurosurgery and Psychiatry.  78:754-756. 2007
    2007 Lrrk2 G2019S substitution in frontotemporal lobar degeneration with ubiquitin-immunoreactive neuronal inclusions.  Acta Neuropathologica.  113:601-606. 2007
    2007 Identification of a novel risk locus for progressive supranuclear palsy by a pooled genomewide scan of 500,288 single-nucleotide polymorphisms.  American Journal of Human Genetics.  80:769-778. 2007
    2007 Progranulin mutations in primary progressive aphasia: The PPA1 and PPA3 families.  JAMA Neurology.  64:43-47. 2007
    2006 The neuropathology of frontotemporal lobar degeneration caused by mutations in the progranulin gene 2006
    2006 Mutations in progranulin are a major cause of ubiquitin-positive frontotemporal lobar degeneration.  Human Molecular Genetics.  15:2988-3001. 2006
    2006 Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17.  Nature.  442:916-919. 2006
    2006 CHMP2B mutations are not a common cause of frontotemporal lobar degeneration.  Neuroscience Letters.  398:83-84. 2006
    2006 A family with tau-negative frontotemporal dementia and neuronal intranuclear inclusions linked to chromosome 17 2006

    Education And Training

  • Mayo Clinic, Jacksonville, Postdoctoral Research
  • Master of Science in Genetic Counseling / Counselor, University of Alabama at Birmingham 2015
  • Doctor of Philosophy in Neuroscience, Mayo Medical School 2012
  • Bachelor of Science or Mathematics in Biology, University of North Florida 2005

    • Full Name

  • Ashley Cannon